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Edexcel SNAB A Level Biology > Topic 6 - Immunity, Infection and Forensics > Flashcards

Topic 6 - Immunity, Infection and Forensics Flashcards

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1
Q

What factors can be used to estimate time of death?

A
  • extent of decomposition
  • stage of succession
  • forensic entomology
  • body temperature
  • rigor mortis/degree of muscular contraction
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2
Q

What is the extent of decomposition, and how can it be used to estimate time of death?

A

Decomposition is carried out by decomposers, break down skin over several weeks, process continues until becomes a skeleton which eventually disintegrates
The rate of decomposition will be affected by factors such as temperature and availability of oxygen. Faster in higher temp, slower in anaerobic conditions

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3
Q

What is the stage of succession and how can it be used to estimate time of death?

A

Changes in type of organisms found on a dead body over time. All of newly arriving species remain (bacteria-fly-larvae-beetles)
The succession stage will differ depending on where the body is located as the accessibility to insects and availability of oxygen

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4
Q

What is forensic entomology, how can this be used to estimate time of death?

A

The study of the colonisation of a dead body by insects. Different insect species will colonise a body at different times after death
Stage of life cycle e.g. blowfly are first to colonise. Factors affecting progression = drugs, humidity, temperature

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5
Q

How can pathologists use forensic entomology to estimate time of death?

A
  • number of species present
  • life cycle stages of insects used
  • succession of insect species
  • life cycle times depend on environmental temperature
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6
Q

What is body temperature and how can this be used to estimate time of death?

A

Body temp = 37 degrees when alive, when dead no metabolic reactions occur. Process of cooling = algor mortis, body temp decreases by 1-2 degrees each hour.
Factors affecting = air temperature, SA:vol ratio, whether clothing is worn

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7
Q

What is rigor mortis, and how can it be used to estimate time of death?

A

Muscles in the body begin to contract about 4-6 hours after TOD, leading to a general stiffening of the body known as rigor mortis.
Process affected by level of muscle development and temperature of surroundings.

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8
Q

What happens to muscle cells in rigor mortis?

A

No more O2 reaches them after death so they begin to respire anaerobically, producing lactic acid. This decreases pH of cells, and denatures enzymes producing ATP. Without ATP, muscles become locked in a contracted state

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9
Q

How useful can body temperature be in providing evidence for time of death?

A
  • only useful for short period of time following death
  • useful if ambient temp known
  • factors affect temp drop (e.g. clothing)
  • drop in body temp after death (algor mortis)
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10
Q

How do decomposers break down dead organic matter?

A

Secrete enzymes that break large organic molecules into smaller ones. CO2 and methane is produced, which are released into the atmosphere and go through the carbon cycle

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11
Q

What can DNA profiling be used for?

A

Identifying individuals, genetic tests (paternity/maternity testing, ancestry kits). Captive breeding programmes to reduce chance of inbreeding

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12
Q

How can DNA profiles be created?

A
  • isolating a sample of DNA
  • multiple copies produced using PCR (use of primers, free nucleotides etc)
  • restriction enzymes to produce DNA fragments
  • carrying out gel electrophoresis of sample created by PCR (electric current/charge applied)
  • analysing resulting pattern of fragments of DNA (fluorescent dye)
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13
Q

Why may evidence from DNA profiles not be absolutely conclusive?

A

DNA profiling has several stages, contamination can occur at any stage.
Only small sections of DNA are analysed, there is the potential for identical profiles for unrelated individuals

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14
Q

What is PCR?

A

The polymerase chain reaction
A common molecular biology technique used to amplify small fragments/sections of DNA and produce large quantities of them

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15
Q

What does PCR require?

A
  • DNA or RNA to be amplified
  • primers
  • DNA/taq polymerase
  • free nucleotides
  • buffer solution
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16
Q

What are the 3 main stages of the PCR reaction?

A
  1. Denaturation - double stranded DNA heated to 95 degrees to break hydrogen bonds holding two strands together
  2. Annealing - temperature decreased to 50-60 degrees so that primers can anneal
  3. Elongation/extension - temperature is increased to 72 degrees so Taq polymerase can build the complementary strands of DNA
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17
Q

Where does PCR occur?

A

In a thermal cycler

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18
Q

What happens to DNA after PCR but before gel electrophoresis?

A

DNA treated with restriction enzymes (breaks it up into different lengths), and fluorescent tags added (enable DNA to be seen under UV light)

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19
Q

How does gel electrophoresis work?

A

DNA fragments are inserted into a well at the end of a piece of agar gel (buffer used). Current applied across gel, and fluorescent dye applied. DNA is negatively charged (phosphate group) so moves towards anode. Different sized molecules move at different speeds (smaller=faster) so mass separates them. UV light shone, pattern of bands can be compared to control

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20
Q

How can DNA profiles be compared?

A

Compare total number of bands, position of bands and size and width of bands

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21
Q

What type of cells are bacteria?

A

Prokaryotes

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22
Q

What are the features of every typical bacterial cell?

A
  • 70S ribosomes
  • cytoplasm lacking membrane bound organelles
  • no nucleus, single circular bacterial chromosome that is free in cytoplasm
  • peptidoglycan cell wall
  • cell membrane with mesosomes
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23
Q

What are features of some, but not all bacterial cells?

A
  • plasmids
  • slimy capsule
  • flagellum
  • pili
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24
Q

What is a virus?

A

Non cellular infectious particle

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25
Q

What is the structure of a virus?

A

Nucleic acid core surrounded by a protein coating known as a capsid.
Some viruses have an outer membrane known as a lipid envelope, with proteins attached (attachment proteins). There are also sometimes enzymes/proteins within the capsid.

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26
Q

What are the differences between the structure of bacteria and viruses?

A
  • bacteria are cells, viruses are not
  • bacteria surrounded by cell wall, viruses by protein capsid
  • bacteria have DNA, viruses can be RNA or DNA
  • bacteria have ribosomes, viruses do not
  • bacterial DNA = circular, viral nucleic acids = linear
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27
Q

How can viruses reproduce?

A

They can only reproduce by infecting living host cells and using their protein building machinery to build new virus particles

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28
Q

What is a disease?

A

An illness or disorder of the body or mind that leads to poor health

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29
Q

What are infectious diseases?

A

Diseases caused by pathogens, which are therefore transmissible and can be spread between individuals of a population

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30
Q

What bacteria causes TB?

A

Mycobacterium tuberculosis

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31
Q

How is TB spread?

A

Through the inhalation of tiny droplets of liquid from the lungs that has been infected by TB bacteria

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32
Q

How does TB cause illness when in the lungs?

A

TB bacteria is engulfed by phagocytes. The bacteria may be able to survive and reproduce (binary fission) while inside phagocytes (due to thick waxy cell wall).
Over time the infected phagocytes will become encased in structures called tubercles in the lungs where the bacteria will remain dormant. The bacteria can later become activated and overpower the immune system, by causing extensive damage to the respiratory system (create cavities in the lungs - untreated lead to respiratory failure). It may spread to other parts of the body and cause organ failure

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33
Q

What are the initial symptoms of TB?

A

Fever, fatigue, coughing, lung inflammation

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34
Q

What is HIV?

A

Human immunodeficiency virus

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35
Q

How does HIV infect human cells?

A

Glycoprotein 120 on HIV attaches to CD4 receptors on T helper cells - allowing HIV to enter the host cell

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36
Q

How is HIV spread?

A

Through bodily fluids
- unprotected sex
- sharing of unsterilized needles
- from mother to child via placenta
- blood donation

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37
Q

How does HIV replicate once in the blood?

A

GP120 glycoproteins on HIV lipid capsule attach to CD4 receptors on T Helper cells.. The capsid enters the T helper cell and releases RNA. Reverse transcriptase converts viral RNA into DNA. Integrase then integrates the viral DNA into the cell DNA/genome, meaning it is transcribed and translated at the cell’s ribosomes. This leads to new viral particles being produced, which leave the T helper cell to infect more T cells, destroying the original cell when they leave via lysis.

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38
Q

What are the initial symptoms of HIV?

A

Flu like

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39
Q

How many RNA strands does HIV contain?

A

2

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40
Q

How does HIV lead to AIDS?

A

After the initial infection period, replication rates drop - this is known as the latency period (no symptoms, possibly for years). Gradually, virus reduces number of T helper cells (B cells no longer activated, no antibodies produced), decreased ability to fight off disease = AIDS

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41
Q

What is AIDS?

A

Acquired immune deficiency syndrome

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42
Q

Why does AIDS lead to death?

A

Patient can no longer produce antibodies against pathogens, become immunocompromised. Unable to fight off infections that would usually be minor (opportunistic diseases). These continue to build up, until advanced AIDS occurs, and this leads to death.

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43
Q

What factors affect how quickly HIV will progress into AIDS?

A
  • access to healthcare
  • age
  • number of existing infections
  • strain of HIV
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44
Q

What is the difference between HIV and AIDS?

A

HIV is a virus, AIDS is the disease caused by HIV

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45
Q

How may HIV and TB be linked?

A

Dormant TB may become an active infection when the immune system is weakened - HIV causes immunodeficiency so there is a positive correlation between the two.

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46
Q

What are the 4 main ways pathogens enter the body?

A
  • broken skin
  • digestive system (contaminated food)
  • respiratory system
  • mucosal surfaces (lining of body cavities)
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47
Q

What are the barriers to infection on the human body?

A

SKIN: physical barrier to infection, blood clotting
MICROORGANISMS OF GUT AND SKIN: flora and fauna compete with pathogens
STOMACH ACID: HCl creates acidic environment which pathogens struggle to survive in
LYSOZYME: secretions of mucosal surfaces, damages bacterial cell walls causing them to burst

48
Q

How does skin flora protect the body from infection?

A

Flora in gut/skin better adapted to conditions
Skin flora prevents the growth of microorganisms by providing competition for space/nutrients/water (outcompete pathogenic organisms)
Release chemicals/toxins to destroy pathogens

49
Q

What is a non specific immune response?

A

When the body reacts/defends itself against a pathogen/microorganism but the response is not dependent on the specific pathogen.
e.g. phagocytosis or inflammation

50
Q

What is infection?

A

When a pathogen/bacteria/microorganism gets inside human tissues or cells

51
Q

What is inflammation and how does it work (responses to histamine)?

A

When the surrounding area of a wound becomes swollen
Mast cells respond to tissue damage by secreting histamine which has the following impacts:
- vasodilation in arterioles to increase blood flow
- increases permeability of capillaries, which become leaky allowing blood plasma to enter tissues

52
Q

What are interferons and how do they work?

A

Anti viral proteins produced by infected cells which diffuses to surrounding cells. This inhibits viral replication to limit formation of new viral particles. Activates WBCs involved with specific immune response, promotes inflammation

53
Q

What is blood clotting and how does it work?

A

Blood clotting is the formation of a clot in a blood vessel. Works to stop the loss of blood and prevent entry of pathogens by providing protective surface for wound healing to occur underneath.
CLOTTING CASCADE!!!

54
Q

What is phagocytosis?

A

The process of engulfing and digesting dead cells and invasive microorganisms

55
Q

How does phagocytosis work?

A

Pathogens produce chemicals that attract phagocytes. Phagocyte recognises pathogen as non self and binds to it. Phagocyte engulfs pathogen to form a phagosome (vacuole) and then the pathogen is broken down by enzymes (phagolysosome) After digestion, phagocyte presents pathogen antigens on cell membrane (can initiate specific immune response!)

56
Q

What is an antigen?

A

Markers on the cell surface membrane that allow cell to cell recognition

57
Q

What are self/non self antigens?

A

Self = antigens produced by organism’s own body cells, do not stimulate immune response
Non self = antigens not produced by an organism’s own body cells, stimulate an immune response

58
Q

What are antigen presenting cells?

A

After pathogens are engulfed by phagocytosis, phagocytes transfer the antigens of the digested pathogen to their cell surface membrane, becoming antigen presenting cells

59
Q

What are antibodies?

A

Y shaped molecules sometimes known as immunoglobins, bind to specific antigens that trigger the specific immune response

60
Q

How do antibodies disable pathogens?

A
  • bind to pathogen receptors to prevent pathogens infecting host cells
  • act as anti toxins by binding to toxins produced by pathogens
  • cause pathogens to clump together (agglutination) so phagocytes can engulf/no spread
61
Q

What is the structure of antibodies?

A

4 polypeptide chains, 2 ‘heavy’ chains attached by disulphide bonds to 2 ‘light’ chains.
Each polypeptide chain has a constant region and a variable region.

62
Q

What is the difference between the constant and variable regions on antibody polypeptide chains?

A

Constant regions - do not vary within a class of an antibody
Variable regions - amino acid sequences different for each antibody. Variable region is where the antibody binds to antigen to form an antibody-antigen complex (unique tertiary structure)

63
Q

What is the importance of the end of a variable region on the end of an antibody?

A

End of variable region = antigen binding site
Varies greatly to give the antibody specificity for binding to the antigen

64
Q

How are membrane bound antibodies different from those secreted into the blood?

A

Membrane bound antibodies are attached to the surface of lymphocytes. Have an extra section of polypeptide chain within their heavy chain to attach to the lymphocyte.
In non bound antibodies, gene can undergo alternative splicing to remove extra section for attachment

65
Q

Where are T cells produced and where do they mature?

A

Produced in bone marrow
Finish maturing in the thymus

66
Q

What do mature T cells have that immature ones do not?

A

Specific cell surface receptors called T cell receptors

67
Q

When/how are T cells activated?

A

When they encounter and bind to their specific antigen on the surface of an antigen presenting cell (macrophage, infected cell or pathogen)

68
Q

What 3 main types of T cells do T cells differentiate into?

A
  • T helper cells: release chemical signalling that help to activate B cells
  • T killer cells: bind to and destroy infected cells displaying relevant specific antigen
  • T memory cells: remain in the blood and enable faster secondary immune response
69
Q

Where do B cells divide and mature?

A

In the bone marrow

70
Q

What are receptors on B cells known as?

A

Antibodies/antibody receptors

71
Q

How are B cells activated?

A

When the corresponding antigen enters the body, B cell binds to antigen forming antigen-antibody complex. The binding of the B cell to its specific antigen, along with the cell signalling molecules produced by T helper cells, activates the B cell

72
Q

What do activated B cells divide into?

A

B effector cells - go on to form plasma cells which produce specific antibodies
B memory cells - remain in blood to enable faster secondary immune response

73
Q

How are antigens presented to immune cells?

A

Phagocytosis - engulfing of pathogens with antigens
Antigen is presented on the surface of an APC
Lymphocytes with receptors that are complementary bind to APC

74
Q

What are post-transcriptional modifications?

A

Modifications made to RNA after it has been synthesised

75
Q

What are the 2 mechanisms of post transcriptional modification?

A
  • splicing
  • alternative splicing
76
Q

What does the structure of the heavy chain of an antibody determine?

A

The functional properties of the antibody - whether an antibody will be bound to the membrane of a white blood cell, or secreted directly into the blood

77
Q

What is pre-mRNA?

A

The mRNA that has been transcribed with both introns and extrons

78
Q

What happens in the process of splicing?

A

Pre-mRNA non coding intron sections are removed and the coding exons are SPLICED together, so the resulting mRNA molecule contains only the coding sequences of the gene

79
Q

What is alternative splicing?

A

The exons of genes can be SPLICED together in many different ways to produce different mature mRNA molecules, and therefore different amino acid sequences. This means that a single eukaryotic gene can code for more than one polypeptide chain

80
Q

What is the primary immune response?

A

The body’s initial response the first time an antigen is encountered by the immune system

81
Q

Why does the primary response take a longer time?

A

The correct T and B cells have to be activated, which takes time, and it can take several days before plasma cells develop and begin antibody production. This means the person will likely experience symptoms upon first time of contracting the disease.

82
Q

What is the secondary immune response?

A

When the immune system encounters an antigen it has already been exposed to

83
Q

Why is the secondary immune response stronger and faster?

A

Due to memory cells being present in large quantities, meaning antibodies are produced more quickly and in larger quantities. This often eliminates the pathogen before symptoms appear

84
Q

What is active immunity?

A

The immunity acquired when an antigen enters the body, triggering a specific immune response

85
Q

What are the two types of active immunity and how are they acquired?

A

Natural (acquired through pathogen exposure) and artificial (acquired through vaccination)

86
Q

What is passive immunity?

A

Immunity acquired without an immune response, antibodies are gained from another source and not produced by the infected person. NO MEMORY CELLS

87
Q

What are the 2 types of passive immunity and how are they acquired?

A

Natural (foetuses receive antibodies across placenta, and babies get them in breast milk) and artificial (injection/transfusion of antibodies e.g. tetanus antitoxin)

88
Q

What is a vaccine?

A

A vaccine contains antigens that are intentionally put into the body to induce artificial active immunity

89
Q

What are the different types of vaccine that can be used?

A

Dead/weakened pathogens, less harmful strains of a pathogen, antigens alone, or a piece of genetic material coding for the antigen

90
Q

Why do vaccines produce long term immunity?

A

They cause memory cells to be produced, so when the antigen is re-encountered there is a stronger secondary response

91
Q

How are clinical trials of a vaccine conducted?

A

Healthy volunteers - test for side effects
Healthy volunteers tested for presence of antibody post vaccination
Group of people at risk of contracting disease given vaccine
Number of people who develop viral disease following vaccination monitored

92
Q

Why might a vaccine be given to immediate family/health workers despite clinical trials being incomplete?

A
  • disease being fatal
  • risk from disease much worse than risk from vaccine
  • health workers are in very close contact, when vaccinated they can care for more people
  • immediate family member vaccination helps reduce the spread
93
Q

What is antigenic variation?

A

When antigens on pathogens change suddenly due to frequent pathogen mutations. This means vaccines may become ineffective as the antigens are no longer recognised by the immune system

94
Q

What is the evolutionary race between pathogens and hosts?

A

As hosts evolve mechanisms to combat pathogens (immune system), pathogens evolve new methods to overcome the immune system.

95
Q

What are the evasion mechanisms of HIV?

A
  • virus kills helper T cells after infecting them, reducing the number of cells that could detect the presence of the virus
  • antigenic variability due to high mutation rate
  • virus prevents infected cells from presenting antigens on cell membrane, making it hard for WBCs to recognise and destroy infected cells
96
Q

How do anti viral drugs work in the treatment of HIV?

A
  • drugs prevent viral replication
  • inhibit reverse transcriptase so viral DNA cannot be formed from viral RNA
  • inhibit integrase so viral DNA cannot integrate into host genome
  • so T helper cells will not be killed
97
Q

What are the evasion mechanisms of mycobacterium tuberculosis?

A
  • disrupt antigen presentation
  • ‘hide’ within phagocytes by preventing lysosome from fusing with phagocytotic vacuole. This means bacteria multiplies within phagocyte
98
Q

Why do dormant TB not get destroyed by the immune system?

A
  • bacteria hide inside macrophages/phagocytes
  • thick waxy cell wall
  • lysosomes cannot fuse with phagocytotic vacuole
  • so bacteria within tubercles cannot be destroyed
99
Q

What are antibiotics?

A

Chemical substances that damage bacterial cells with little or no harm to human tissue

100
Q

Who discovered the first antibiotic?

A

Alexander Fleming - penicillin

101
Q

What are the two types of antibiotics?

A

Bactericidal - kill bacterial cells
Bacteriostatic - inhibit bacterial cell multiplication/growth

102
Q

What are some of the mechanisms antibiotics use to disrupt bacterial cell growth and division?

A
  • inhibition of bacterial wall synthesis
  • inhibition of protein synthesis - stops enzyme production and therefore metabolic processes
  • damaging cell membranes (leads to lysis)
  • inhibition of nucleic acid synthesis, replication and transcription
103
Q

Why are mammalian cells not damaged by antibiotics?

A

They are eukaryotic, so don’t have cell walls, and have different enzymes and ribosomes

104
Q

Why are viruses not affected by antibiotics?

A

Do not have cellular structures such as enzymes, ribosomes and cell walls

105
Q

What are hospital acquired infections (HAIs)?

A

Infections contracted by a patient while in hospital

106
Q

What is the transmission of HAIs increased by, what are some examples?

A

Poor hygiene practices e.g.
- staff and visitors not washing hands regularly
- uncontained coughing and sneezing
- failing to disinfect equipment and surfaces after use

107
Q

What measures do hospitals have in place to reduce the spread of HAIs?

A
  • staff and visitors must wash hands regularly when visiting patients
  • if a person contracts a HAI, they should be moved to an isolation ward
  • surfaces and equipment should be disinfected after every use
108
Q

What are the risks of antibiotic resistant HAIs?

A
  • difficult to treat as do not respond to regular antibiotics
  • therefore can cause serious health complications of deaths
109
Q

Why is the risk of antibiotic resistant bacterial strains arising high in hospital environment?

A

Antibiotics are widely used in hospitals which provides a selection pressure for resistant strains of bacteria to develop. This drives natural selection

110
Q

What hospital practices have been developed to reduce the risk of antibiotic resistant HAIs?

A
  • no antibiotic prescriptions for minor infections or viral diseases
  • no use of antibiotics as a preventative measure
  • prescription of a narrow spectrum antibiotic to treat the infection (prevents transfer of resistance genes)
  • rotate the use of different antibiotics to decrease chance of bacterial resistance
111
Q

How does antibiotic resistance in bacteria arise?

A
  • antibiotic resistance arises in an individual by random mutation
  • treatment by antibiotics kills most of non resistant individuals
  • resistant survives, passes on mutation for antibiotic resistance via binary fission
  • antibiotic resistance increases in frequency in the population
112
Q

What is the role of DNA primers in produced amplified sequences?

A

Primers have a specific base sequence, so they bind to complementary bases at the ends of DNA to be amplified. Therefore, they provide a site for DNA polymerase to bind.

113
Q

What changes occur inside a body in the first week after death?

A
  • rigor mortis
  • body temperature falls
  • autolysis/breakdown of cells by enzymes
  • putrefaction/discolouring/bloating
114
Q

What is the effect of ambient temperature on rate of decomposition?

A

Increase in temperature increases rate of decay as there is an increase in enzyme activity and growth of microorganisms

115
Q

How does the evolutionary race affect the body’s specific immune response to infection by viruses?

A
  • mutation occurs in the nucleic acid, changing antigens on viral surface
  • secondary immune response not possible
  • as memory cells no longer recognise the new antigen
  • another primary response is needed
116
Q

How does the evolutionary race affect antigen presentation to T helper cells?

A
  • mutation occurs in the bacterial DNA, leading to a change in the antigen on the surface
  • memory T cells will not recognise the antigen
  • another primary immune response is needed
  • to activate more T helper cells
117
Q

Why are there relatively few species of bacteria in the stomach?

A

Hydrochloric acid denatures bacterial enzymes
Bacteria that do live in the stomach have adaptations/mutations which enable survival

Edexcel SNAB A Level Biology (9 decks)

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